The mouse mammary tumor virus (MuMTV) causes mammary adenocarcinomas. In the terminology of tumor biology, the virus confers a selective advantage on the infected cell. Mammary tumors in BALB/cfC3H mice are characterized by amplification of MuMTV genes and monoclonal proliferation of cells. We postulate that infection with MuMTV results in a change in the mammary epithelial genome which confers a dose-dependent selective advantage on the infected cell. Cells which acquire additional MuMTV DNA sequences have incremental advantages and progress to emerge from the general population as autonomous (malignant) monoclonal outgrowths. It is the object of the research proposed here to experimentally test this hypothesis, its alternatives and logical extensions by studying the number, character and position of acquired MuMTV genes in detail using nucleic acid hybridization and restriction endonuclease mapping techniques and to correlate this data with the biology of the mouse mammary tumor system.